The findings demonstrated that RSPO3 plays a crucial role in regulating NSCLC radioresistance via NLRP3 mediated pyroptosis. Targeting the RSPO3-NLRP3 inflammasome axis may offer a potential therapeutic strategy to enhance the efficacy of radiotherapy for NSCLC patients.
Our findings suggest that increased methylation and decreased expression of RSPO3 may indicate a poor prognosis in CCA. Restoring RSPO3 expression by targeting promoter DNA demethylation could offer insights for precise treatment of CCA.
Moreover, the inhibitory effect of R-spondin 3 on the expressions of VCAM-1, ICAM-1 and MCP-1 in high glucose-treated HUVECs could be blocked by knockdown of leucine-rich G protein coupled receptor 4 (LGR4, R-spondin 3 receptor) or the specific inhibitor of Wnt/β-catenin pathway. Taken together, R-spondin 3 could suppress high glucose-induced endothelial activation through LGR4/Wnt/β-catenin pathway.